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Release of Vesicular Stomatitis Virus Spike Protein G-Pseudotyped Lentivirus from the Host Cell Is Impaired upon Low-Density Lipoprotein Receptor Overexpression.低密度脂蛋白受体过表达时，水泡性口炎病毒刺突蛋白G假型慢病毒从宿主细胞的释放受损。
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Molecular Dynamics Simulation Reveals Exposed Residues in the Ligand-Binding Domain of the Low-Density Lipoprotein Receptor that Interacts with Vesicular Stomatitis Virus-G Envelope.分子动力学模拟揭示了与水疱性口炎病毒-G 包膜相互作用的低密度脂蛋白受体配体结合域中的暴露残基。
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本文引用的文献

1
LDL receptor and its family members serve as the cellular receptors for vesicular stomatitis virus.LDL 受体及其家族成员是水疱性口炎病毒的细胞受体。
Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):7306-11. doi: 10.1073/pnas.1214441110. Epub 2013 Apr 15.
2
LDLR-Gene therapy for familial hypercholesterolaemia: problems, progress, and perspectives.家族性高胆固醇血症的低密度脂蛋白受体基因治疗：问题、进展与展望
Int Arch Med. 2010 Dec 13;3:36. doi: 10.1186/1755-7682-3-36.
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The role of calcium in lipoprotein release by the low-density lipoprotein receptor.钙在低密度脂蛋白受体释放脂蛋白中的作用。
Biochemistry. 2009 Aug 4;48(30):7313-24. doi: 10.1021/bi900214u.
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Molecular architecture of the bipartite fusion loops of vesicular stomatitis virus glycoprotein G, a class III viral fusion protein.水泡性口炎病毒糖蛋白G（一种III类病毒融合蛋白）二分融合环的分子结构。
J Biol Chem. 2008 Mar 7;283(10):6418-27. doi: 10.1074/jbc.M708955200. Epub 2007 Dec 28.
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Role of LAMP-2 in lysosome biogenesis and autophagy.LAMP-2在溶酶体生物发生和自噬中的作用。
Mol Biol Cell. 2002 Sep;13(9):3355-68. doi: 10.1091/mbc.e02-02-0114.
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Hassles with taking out the garbage: aggravating aggresomes.倒垃圾带来的麻烦：加剧聚集体。
Traffic. 2002 Jun;3(6):388-96. doi: 10.1034/j.1600-0854.2002.30602.x.
7
A mutation of the Wilson disease protein, ATP7B, is degraded in the proteasomes and forms protein aggregates.威尔逊病蛋白ATP7B的一种突变体在蛋白酶体中被降解并形成蛋白质聚集体。
Gastroenterology. 2001 Mar;120(4):967-74. doi: 10.1053/gast.2001.22543.
8
Vesicular stomatitis virus G protein acquires pH-independent fusion activity during transport in a polarized endometrial cell line.水泡性口炎病毒G蛋白在极化子宫内膜细胞系中运输期间获得pH非依赖性融合活性。
J Virol. 1999 Dec;73(12):10447-57. doi: 10.1128/JVI.73.12.10447-10457.1999.
9
Level of ICAM-1 surface expression on virus producer cells influences both the amount of virion-bound host ICAM-1 and human immunodeficiency virus type 1 infectivity.病毒产生细胞上细胞间黏附分子-1（ICAM-1）的表面表达水平既影响病毒体结合的宿主ICAM-1的量，也影响1型人类免疫缺陷病毒的感染性。
J Virol. 1998 Nov;72(11):9329-36. doi: 10.1128/JVI.72.11.9329-9336.1998.
10
Stable and efficient gene transfer into the retina using an HIV-based lentiviral vector.使用基于HIV的慢病毒载体将基因稳定高效地导入视网膜。
Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10319-23. doi: 10.1073/pnas.94.19.10319.

低密度脂蛋白受体过表达时，水泡性口炎病毒刺突蛋白G假型慢病毒从宿主细胞的释放受损。

Release of Vesicular Stomatitis Virus Spike Protein G-Pseudotyped Lentivirus from the Host Cell Is Impaired upon Low-Density Lipoprotein Receptor Overexpression.

作者信息

Otahal Alexander, Fuchs Renate, Al-Allaf Faisal A, Blaas Dieter

机构信息

Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, Vienna Biocenter, Vienna, Austria.

Department of Pathophysiology, Medical University of Vienna, Vienna, Austria.

出版信息

J Virol. 2015 Nov;89(22):11723-6. doi: 10.1128/JVI.01869-15. Epub 2015 Sep 2.

DOI:10.1128/JVI.01869-15
PMID:26339060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4645664/
Abstract

Production of a vesicular stomatitis virus spike protein G (VSVG)-pseudotyped lentiviral expression vector in HEK293 cells decreased on overexpression of low-density lipoprotein receptor (LDLR) but not that of ICAM1 or TfR1. Reverse transcription-quantitative PCR (RT-qPCR) revealed a reduction in vector RNA as a function of LDLR expression. Decreased syncytium formation suggested diminished surface expression of VSVG. Intracellular VSVG granules colocalized with LDLR, ER-Golgi intermediate compartment protein 53 (ERGIC53), LAMP2, and vimentin but not with GM130 or calnexin, suggesting that VSVG interacts with LDLR within the ERGIC, resulting in rerouting into the aggresome/autophagosome pathway.

摘要

在HEK293细胞中，低密度脂蛋白受体（LDLR）的过表达会降低水泡性口炎病毒刺突蛋白G（VSVG）假型慢病毒表达载体的产生，但细胞间黏附分子1（ICAM1）或转铁蛋白受体1（TfR1）的过表达则不会。逆转录定量PCR（RT-qPCR）显示载体RNA随LDLR表达而减少。合胞体形成减少表明VSVG的表面表达减少。细胞内VSVG颗粒与LDLR、内质网-高尔基体中间区室蛋白53（ERGIC53）、溶酶体相关膜蛋白2（LAMP2）和波形蛋白共定位，但不与GM130或钙连蛋白共定位，这表明VSVG在内质网-高尔基体中间区室（ERGIC）内与LDLR相互作用，导致重新路由到聚集体/自噬体途径。